Experiments will be performed to investigate the mechanisms of endotoxin-induced regression of established, syngeneic murine tumors. The likelihood that regression is dependent on T-cell-mediated immunity will be investigated directly by determining whether intravenous infection of sensitized T-cell will facilitate regression by endotoxin of susceptible tumors growing in T-cell-deficient recipients. The subclass identification of the responsible T-cells will be determined by use of appropriate antisera to T-cell surface markers. That the ultimate effector mechanism is a non-specific one expressed by macrophages or NK cells will be investigated by employing a model of endotoxin-induced regression in which a local intratumor immune response to Corynebacterium parvum substitutes for tumor specific immunity. Different types of host cells present in a cell suspension of enzyme digested regressing tumors will be purified by sequential "planning" on plastic dishes coated with antibodies to cell surface markers and each type of host cell assayed in vitro for its antitumor function. Similar procedures will be employed to identify the host cells responsible for the regression of ascites tumors which follows combination treatment with cytoxan and endotoxin. The possibility that interferon is involved in the mechanism of tumor regression will be investigated by determining whether T-cell-mediated priming for endotoxin-induced regression also primes for increased interferon production.